AbstractBACKGROUND:
Gastroparesis (GP) is a disabling chronic gastroenterologic disorder with high morbidity that severely impacts patients' quality of life. GP can present acutely after a viral-like gastrointestinal illness resulting in speculation that in some patients, neurologic damage caused by the infection might underlie the pathogenesis of idiopathic gastroparesis (IGP).

AIMS:
The aim of this study is to document case reports of Enterovirus (EV) infection as a possible cause of IGP.

METHODS:
Eleven patients referred with a diagnosis of GP underwent workup to exclude known causes of GP. Those with a history of flu-like symptoms or gastroenteritis prior to onset of GP symptoms had gastric biopsies taken during upper endoscopy to assess for the presence of gastric mucosal EV infection. Data on presenting symptoms, extra-intestinal symptoms and conditions, prior nutritional support requirements, upper endoscopy findings, and response to therapy were cataloged.

RESULTS:
Eleven patients were diagnosed as IGP. Nine had active EV infection on gastric biopsies and were included (7/9 female, mean age 43 years). Eight out of nine received EV treatment with antivirals and/or immune therapies, with a wide degree of variability in treatment regimens. Four out of eight who received EV treatment had symptomatic improvement. One patient had stable symptoms. Three patients are currently undergoing therapy.

CONCLUSIONS:
Gastric EV infection was frequently detected (82 %) in patients undergoing investigation for IGP. Antiviral and/or immune therapies against EV seem to be favorable, as most of our patients had resolution of their GP symptoms after treatment. This is the first study to identify EV as a possible infectious etiology of IGP.

Results
Eleven patients were diagnosed as IGP and, based on history of prior infection preceding the onset of their symptoms, underwent further testing for gastric EV infection. Nine (82 %) were found to have active EV infection on gastric biopsies (with positive staining of gastric mucosa), and those were the patients subsequently included in the study. Seven (78 %) were female with a mean age of 43 years (Table 1). Heartburn was the most common upper GI symptom in 67 % of patients followed by nausea/ vomiting (44 %), and constipation was the most commonly reported lower GI symptom in 56 %. Seven (78 %) patients had extra-intestinal symptoms and conditions associated with their IGP, such as autonomic dysfunction confirmed by tilt table testing (56 %), and myalgic encephalomyelitis/chronic fatigue syndrome (56 %). Three (33 %) patients required total parenteral nutrition, and two (22 %) required gastric pacemaker placement.

On upper endoscopy, 78 % of patients had endoscopic findings of mucosal erythema and edema described as gastropathy. Of the nine included patients with gastric biopsies positive for EV, eight (89 %) received EV treatment with antivirals and/or immune therapies, with a wide degree of variability in treatment regimens (Table 2). One patient elected not to undergo treatment for EV infection as they had a marked response to domperidone therapy with control of their symptoms.

Very interesting, especially that half the patients given antiviral treatments had improvements in their gastroparesis (delayed gastric emptying). Although the antiviral treatments were somewhat hotchpotch. The full paper details the antiviral treatments received:

Four of eight patients (50 %) who received EV treatment had symptomatic improvement (Table 2). Their treatment regimens were as follows: One treated with intravenous immunoglobulin (IVIG) alone; one treated with IVIG, ribavirin, Isoprinosine, Equilibrant®, CoQ-10, and EnteraGam®; one treated with IVIG, Isoprinosine, Equilibrant®, and CoQ-10; and one treated with EnteraGam® and naltrexone.

[In summary, our studies provided evidence for the pathogenic role of enteroviral dsRNA in the stomach biopsies of patients who had FD/chronic gastritis with and without ME/CFS. Much more research will be needed to define the mechanism of virus-mediated tissue injury and host responses. Development of antiviral therapy against enteroviruses and/or dsRNA cannot be overemphasized, and the importance of enteroviruses in FD/chronic gastritis can only be realized with a randomized, placebo-controlled antiviral drug trial.

Seems the same similarities have thought to apply Type 1 Diabetes for a while too.

http://diabetes.diabetesjournals.org/content/61/3/687
[Enterovirus RNA was found in diabetic patients more frequently than in control subjects and was associated with a clear inflammation response in the gut mucosa. Viral RNA was often detected in the absence of viral protein, suggesting defective replication of the virus. Patients remained virus positive in follow-up samples taken after 12 months’ observation. The results suggest that a large proportion of type 1 diabetic patients have prolonged/persistent enterovirus infection associated with an inflammation process in gut mucosa. This finding opens new opportunities for studying the viral etiology of type 1 diabetes.]

Enteroviruses were found not only in intestinal mucous linings but also in so-called nerve cell ganglia in deeper segments of the intestinal wall. Receptors for a group of enteroviruses were also found in both the intestinal mucous linings and nerve cell ganglia, which may explain how the virus can make its way into the nerve system in the intestine.

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because enterovirus in the nervs occupying receptors in the nerv cells could change the function of signaling molecules, and therefore create chronic inflammation.

Dr Chia was of a similar opinion in a study into those both with and without ME/CFS

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Have you ever ventured to try any anti-enterovirus treatments, @kangaSue, on the assumption that your gastroparesis may be due to enterovirus?

Oxymatrine / Equilibrant might be worth looking into, as that's Dr Chia's most effective enterovirus treatment; I actually tried oxymatrine speculatively for my ME/CFS even before I was able to get a blood test to confirm I had chronic enterovirus. This you can buy online as a supplement.

Dr Chia also uses Epivir, which he finds produces mild benefits in around 1 in 3 enterovirus ME/CFS patients.

Ribavirin is a more potent enterovirus antiviral, but long term use is inadvisable because of toxicity.

More recently Chia has been trying tenofovir, and antiviral and immunomodulator.

I was looking into interferon alpha suppositories to treat enterovirus. Dr Chia used IV interferon for ME/CFS patients with some success, but Western IV interferon is very expensive, around $5000 per month. However, for around $10 you can buy cheap Russian interferon alpha suppositories.

Have you ever ventured to try any anti-enterovirus treatments, @kangaSue, on the assumption that your gastroparesis may be due to enterovirus?

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I've been on a different track of late as to the cause of my gastroparesis after discovering for myself that some of my imaging studies were clearly showing Nutcracker Syndrome (NCS - left renal vein compression) but it was missed by all the supposed medical professionals.

It's a long story but about 20% of those with this have severe autonomic dysfunction (in having POTS) and plenty of others have a lesser involvement with low bp, GI problems and Autonomic Neuropathy, with or without the more typical other symptoms of NCS, which fits for me, and fixing the renal vein compression is also relieving these other symptoms in many cases.

I don't identify as having ME/CFS but interestingly, I have come across a numer of people in other forums who eventually found that they had NCS after first being diagnosed with ME/CFS instead.

I gave up on pursuing an enterovirus cause when repeated pleas to my GI to do some full thickness biopsies of the GI tract fell on deaf ears. I was hoping to send samples off to the Enterovirus Foundation for testing but because they found intestinal ischemia damage during a colonoscopy (and it resulted in having a perforated bowel from the scope), I was deemed too high a risk to have any biopsies taken in future, either the standard variety or full thickness one's.

For the same reason, they now won't contemplate doing the major surgery required to fix the renal vein compression either. Everyone is quoting their favourite mantra and "get out" clause at me, "first, do no harm." As you can imagine, that approach is not doing much to alleviate my symptoms!